ArticleOncology letters2019
Effects of cisatracurium on epithelial-to-mesenchymal transition in esophageal squamous cell carcinoma.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Hsa_circ_0000467 promotes colorectal cancer proliferation and stem cell characteristics by activating the TCF4/Wnt/β-catenin pathway via sponging miR-520g.APL bioengineering · 2025Article
- RGS1 serves as an antitumor target to inhibit proliferation of NICN87-DR cells and tumor growth in the gastric cancer mouse model.Turkish journal of biology = Turk biyoloji dergisi · 2022Article
- Exosomal miR-4800-3p Aggravates the Progression of Hepatocellular CarcinomaFrontiers in oncology · 2022Article
- Cisatracurium besilate enhances the TRAIL-induced apoptosis of gastric cancer cells via p53 signaling.Bioengineered · 2021Article
- Cisatracurium inhibits the growth and induces apoptosis of ovarian cancer cells by promoting lincRNA-p21.Bioengineered · 2021Article
- Long non‑coding RNA PITPNA‑AS1 silencing suppresses proliferation, metastasis and epithelial‑mesenchymal transition in non‑small cell lung cancer cells by targeting microRNA‑32‑5p.Molecular medicine reports · 2021Article
- Possible involvement of TGF‑β‑SMAD‑mediated epithelial‑mesenchymal transition in pro‑metastatic property of PAX6.Oncology reports · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive types of cancer worldwide, with a poor prognosis. The aim of the present study was to investigate the effect of cisatracurium (Cis) on epithelial-to-mesenchymal transition (EMT) in ESCC and its potential mechanism of action. In the present study, Cis was used to treat ECA-109 cells, with cell proliferation measured by a Cell Counting Kit-8 assay and the expression of TGF-β and phospho-Smad2/3 detected by western blotting. TGF-β was then applied to induce EMT. Flow cytometry, wound healing and Transwell assays were used to evaluate cell proliferation, apoptosis, invasion and migration. In addition, cell cycle-related proteins, including cyclin D1, p53 and p21, and EMT-associated proteins, including E-cadherin (E-cad), N-cadherin (N-cad), Vimentin and Slug, were examined by western blot analysis. The results revealed that Cis inhibited the proliferation and promoted apoptosis of ESCC cells. Following treatment with Cis, the expression of TGF-β and phosphorylation of Smad2/3 were downregulated. Cis also suppressed cancer cell invasion and migration induced by TGF-β. In addition, the expression levels of cyclin D1 were decreased, accompanied by increased p53 and p21 expression. In addition, the expression level of E-cad was increased, whereas N-cad, Vimentin and Slug were significantly reduced. Taken together, the results of the present study revealed that exposure of ESCC cells to Cis inhibited EMT and reduced cell invasion and metastasis through the TGF-β/Smad signaling pathway.
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